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RAGE-AB Interactions in the Pathophysiology of Alzheimer's Disease
dc.contributor.author | Yan, Shirley ShiDu | |
dc.contributor.author | Stern, David M. | |
dc.contributor.author | Kane, Michael D. | |
dc.contributor.author | Kuo, Yu-Min | |
dc.contributor.author | Lampert, Heather C. | |
dc.contributor.author | Roher, Alex E. | |
dc.date.accessioned | 2015-05-28T15:37:53Z | |
dc.date.available | 2015-05-28T15:37:53Z | |
dc.date.issued | 1998 | |
dc.identifier.citation | Yan, Shirley ShiDu, David Stern, Michael D. Kane, Yu-Min Kuo, Heather C. Lampert, and Alex E. Roher. "RAGE-AB Interactions in the Pathophysiology of Alzheimer's Disease." Restorative Neurology and Neuroscience 12.2,3 (1998): 167-73. Web. 28 May 2015. | en_US |
dc.identifier.uri | http://hdl.handle.net/1808/17866 | |
dc.description | This is the published version. Copyright 1998 IOS Press. | en_US |
dc.description.abstract | RAGE is a cell surface molecule primarily identified for its capacity to bind advanced glycation end-products and amphoterin. Immunocytochemical studies demonstrated that in Alzheimer's Disease (AD) the expression of RAGE is elevated in neurons close to neuritic plaque beta-amyloid (AB) deposits and in the cells of AB containing vessels. Cross-linking of surface bound AB 1-40 to endothelial cells, yielded a band of 50 kDa identified as RAGE. Using the soluble extracellular domain of recombinant human RAGE, we found that AB binds to RAGE with a Kd = 57 ± 14 nM, a value close to those found for mouse brain endothelial cells and rat cortical neurons. The interaction of AB with RAGE in neuronal, endothelial, and RAGE-transfected COS-1 cells induced oxidative stress, as assessed by the TBARS and MTT assays. ELISA demonstrated a 2.5 times increase of RAGE in AD over control brains. Activated microglia also showed elevated expression of RAGE. In the BV-2 microglial cell line, RAGE bound AB in dose dependent manner with a Kd of 25 ± 9 nM. Soluble AB induced the migration of microglia along a concentration gradient, while immobilized AB arrested this migration. AB-RAGE interaction also activated NF-kB, resulting in neuronal up-regulation of macrophage-colony stimulating factor (M-CSF) which also induced microglial migration. Taken together, our data suggest that RAGE-AB interactions play an important role in the pathophysiology of Alzheimer's Disease. | en_US |
dc.publisher | IOS Press | en_US |
dc.title | RAGE-AB Interactions in the Pathophysiology of Alzheimer's Disease | en_US |
dc.type | Article | |
kusw.kuauthor | Yan, Shirley ShiDu | |
kusw.kudepartment | Pharmacology & Toxicology | en_US |
kusw.oaversion | Scholarly/refereed, publisher version | |
kusw.oapolicy | This item does not meet KU Open Access policy criteria. | |
dc.rights.accessrights | openAccess |
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Pharmacy Scholarly Works [299]